Selegeline, Carnitines, Galantamine, and CoQ10 for Parkinson’s

Q First of all, thank you for your website. It is truly a very helpful and hope-building site.

My 70 year-old mother has suffered from Parkinson’s disease dementia for almost 10 years and has just recently found out that she carries the gene mutation for frontal-temporal dementia with ALS.

I am really desperate to know which supplements would benefit her for both the movement disorder and the dementia, but I don't know which category to search under, dementia, Parkinson's or ALS, etc.

Would you help me figure out what to give her?

Tara, Edmonton, AB, Canada

Dear Tara,

I assume that your mother has been treated with Sinemet (a combination of L-dopa and carbidopa). Has she ever taken Selegeline (Deprenyl)? Selegeline is an adjunctive treatment for Parkinson’s, which restores dopaminergic receptor sensitivity, thereby enhancing the effects of Sinemet. I recommend starting with 5 mg in the morning, advancing to a second 5 mg dose at noon.

Parkinson’s disease (PD) symptoms have been helped by the carnitines, especially propionyl-L-carnitine. Researchers have found that the carnitines can enhance walking in both animals and humans.1 Propionyl-L-carnitine has been found to be valuable for muscles.2Acetyl-L-carnitine has also been shown to be of benefit in those with ALS. A good formulation to take would use both propionyl-L-carnitine and acetyl-L-carnitine, plus a generous dose of alpha lipoic acid.

Galantamine has also surprisingly been shown to be of benefit in Parkinson’s. Researchers in Norway and the United States conducted a trial to assess the ability of galantamine to alleviate the symptoms of dementia in patients with Parkinson’s disease.3

For the first 4 weeks of the study, the patients received 4 mg/day of galantamine, and 8 mg/day for the last 4 weeks. 13 patients completed the trial. Cognition improved in eight patients (62%), but worsened in four (31%), with one unchanged.

Parkinson’s disease is not usually associated with the cholinergic deficits that agents such as galantamine are designed to remedy. Nevertheless, the galantamine treatment brought about improvement in the symptoms of Parkinsonism in six patients (46%)—and in three of these patients, the improvement was described as “marked.” In three patients (23%), the symptoms worsened mildly (mainly a worsening of tremor), and four patients (31%) remained unchanged.

These findings suggest that treatment with galantamine can improve cognition, hallucinations, and even motor symptoms in patients with PD and dementia. Thus, the sphere of galantamine’s influence appears to encompass Parkinson’s disease itself, not just the dementia that develops with advanced Parkinson’s, thanks to galantamine’s ability to modulate those vital nicotinic receptors in the human brain.

Another study of 80 patients in the early stages of PD (early enough that they did not yet require treatment for their disability) examined the ability of Coenzyme Q10 to slow the progression of Parkinson’s.4 The patients were assigned to one of four groups, receiving either placebo or 300 mg, 600 mg, or 1200 mg of CoQ10 per day; in addition, each group received 1200 IU of vitamin E per day.

The exciting result of this research is that all three of the CoQ10 doses decreased the rate of functional decline in the Parkinson’s patients, with the greatest effect being observed at the highest dosage, 1200 mg/day. The mental score also showed improvement with increasing dosage.

The doses of CoQ10 used in this study were much higher than those used in other clinical studies. For example, an effective dose used in many heart disease studies ranges from 50 to 200 mg/day. The most likely explanation for the difference in dosage requirements is that CoQ10’s access to the brain is impeded somewhat by the blood-brain barrier (a brain-capillary membrane that protects the brain from most molecular invaders). Thus, higher blood levels of CoQ10 may be required for this nutrient to reach the brain than to reach the heart, which has no such barrier.

Although CoQ10 provided significant benefits to the Parkinson's patients, the results were not immediate. After 1 month, the 1200-mg/day group showed a benefit. It took 4 months of daily treatment, however, before a clear separation emerged between the 1200-mg/day group and the control, and 8 months before such a separation emerged between the 300- and 600-mg/day groups and the control group. At the end of the 16-month trial, the change in all measurements was most significant in the 1200-mg/day group.

Another nutrient that has been used with benefit by many Parkinsonian patients is the antioxidant, ­glutathione. I suggest taking it in encapsulated nanospheres, or the more affordable glutathione precursor, N-Acetylcysteine, in a dose of 600 mg three times daily—or a combination of the two.

I hope these suggestions will be of help,

Ward Dean, M.D.

References

  1. Brevetti G, di Lisa F, Perna S, Menabó R, Barbato R, Martone VD, Siliprandi N. Carnitine-related alterations in patients with intermittent claudication: indication for a focused carnitine therapy. Circulation. 1996 May 1;93(9):1685-9.
  2. Smith WA, Fry AC, Tschume LC, Bloomer RJ. Effect of glycine propionyl-L-carnitine on aerobic and anaerobic exercise performance. Int J Sport Nutr Exerc Metab. 2008 Feb;18(1):19-36.
  3. Aarsland D, Hutchinson M, Larsen JP. Cognitive, psychiatric, and motor response to galantamine in Parkinson’s disease with dementia. Int J Geriatr Psychiatry. 2003;18:937-41.
  4. Shults CW, Oakes D, Kieburtz K, et al. Effects of coenzyme Q10 in early Parkinson disease: evidence of slowing of the functional decline. Arch Neurol. 2002;59:1541-50.

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